Abstract
Cellular quality control systems have gained much attention in recent decades. Among these, autophagy is a natural self-preservation mechanism that continuously eliminates toxic cellular components and acts as an anti-ageing process. It is vital for cell survival and to preserve homeostasis. Several cell-type-dependent canonical or non-canonical autophagy pathways have been reported showing varying degrees of selectivity with regard to the substrates targeted. Here, we provide an updated review of the autophagy machinery and discuss the role of various forms of autophagy in neurodegenerative diseases, with a particular focus on Parkinson’s disease. We describe recent findings that have led to the proposal of therapeutic strategies targeting autophagy to alter the course of Parkinson’s disease progression.
Highlights
We focus on the involvement of autophagy in Parkinson’s disease (PD), we comment on the major unanswered questions in the field and propose new directions for possible therapeutic interventions targeting autophagy pathways
Regardless of the roles played by the different types of autophagy in PD, lysosomes play a central role in α-syn degradation
In the specific context of PD, we reviewed above some of the key results indicating that targeting the mitophagy and chaperone-mediated autophagy (CMA) pathways could be a means to protect against α-syn-related toxicity (Appendix B provides a general significance statement)
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. PD is characterized by a broad spectrum of motor and non-motor signs and symptoms They include rest tremor, bradykinesia, postural instability/unsteady gait, rigidity, alongside psychiatric disorders, sleep disorders, dysautonomic disorders, pain, anosmia, and cognitive disorders. The symptoms of PD develop gradually with age They can start with a slight tremor in one hand and a feeling of stiffness in the body; bradykinesia is frequent. The genes most frequently linked to PD include GBA, LRRK2, PRKN, SNCA, ATP13A2, ATP10B, DJ-1, DNAJC6, FBXO7, HTRA2, MAPT, PINK1, PLA2G6, VPS35, and VPS13C [4,7,8,9,10,11,12,13]. Other genetic alterations have been associated with PD, including epigenetic changes, such as DNA methylation, chromatin remodeling, histone modifications, microRNAs and long non-coding RNAs [4,14]
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